The purpose was to determine whether chronic exposure to moderate to high blood levels of acetate would result in alterations of expression of selected membrane markers. For this purpose, we examined alcoholic subjects exposed to acetate via alcohol metabolism (up to 10 fold physiological levels) and hemodialysis patients exposed via the dialysis buffers (up to 100 fold physiological levels). Acute exposure to high levels of alcohol was reported by others to enhance the expression of HLA class I antigens. In the present study, the expression of HLA class I (ABC), Class II (Dr) and CD16 Fc receptor antigens were measured by flow cytometry on blood leukocytes from alcoholic and hemodialyzed uremic patients. By staining with fluor=labeled monoclonal antibodies, we detected a small but not significant increase in expression (intensity) of HLA class I antigens on lymphocytes and monocytes of alcoholic subjects in comparison with a reference population of normal controls. Hemodialysis subjects exhibited a decreased expression of HLA class I. Alcoholic and hemodialysis subjects both showed a significant decrease in expression of HLA class II antigens. The average percentage of lymphocytes from alcoholics that expressed CD16 was similar to that of controls. Hemodialyzed subjects exhibited a decrease percent of lymphocytes that stained for CD16 but an increase percent of monocytes that stained for CD16. The results were compatible with a hypothesis that altered expression of HLA class I reported by others was an alcohol effect while the altered expression of class II and CD16 that we observed was an effect caused by uremia, but not by acetate.